Journals / Gazi Medical Journal / 2009 / Cilt: 20 - Sayı: 2

Vincristine induced survivin expression in the human multiple myeloma cell line ARH77

İnsan multiple myeloma hücre dizisi ARH77’de vinkristinin survivin gen ifadesi üzerine etkisi

Pages
72–75
Publication Date
2022-10-19
DOI
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⚡ TL;DR(Too Long; Didn't Read)

Survivin expression significantly increased after 48 and 72 h (p

📌 3 Key Takeaways

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Objective & Hypothesis:Purpose: Survivin, an inhibitor of the apoptosis (IAP) gene family, is a mitotic protein with actions on various cellular events such as cell division, apoptosis, and cellularresponse to stress.
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Key Findings & Data:We aimed to detect theexpression pattern of survivin in vincristine treated MM cell line ARH77.
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Conclusion & Impact:Survivin expression significantly increased after 48 and 72 h (p
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Purpose: Survivin, an inhibitor of the apoptosis (IAP) gene family, is a mitotic protein with actions on various cellular events such as cell division, apoptosis, and cellularresponse to stress. Vincristine, a chemotherapeutic agent used in multiple myeloma(MM), induces apoptosis via inhibition of spindle formation. We aimed to detect theexpression pattern of survivin in vincristine treated MM cell line ARH77. Materials and Methods: Vincristine was added to human multiple myeloma cellline ARH77 cultures for 24, 48, 72, and 96 h and 10-7 to 10-10 M concentrations. Sur- vivin expression was determined by quantitative RT-PCR. Statistical comparisons ofratios were made with two proportions z test. Results: We did not observe an increase in survivin expression after 24 or 96 h oftreatment. Survivin expression significantly increased after 48 and 72 h (p

Özet

Amaç: Apoptozis İnhibitör Gen ailesinin (IAP) bir üyesi olan survivin, hücre bölünmesi, apoptozis ve strese hücresel yanıt gibi birçok olayda rol oynayan mitotikbir proteindir. Multiple myelomada (MM) temel kemoterapi ajanlarından biri olanvinkristin, hücrelerde mikrotubül olusumunu engelleyerek apoptozisi uyarmaktadır.Bu çalısmada, MM hücre dizisi ARH77 hücrelerinde vinkristinin doz ve süre bağımlı olarak uygulanması ile survivin gen ifadesi üzerinde olusturabileceği değisiklikleri incelemeyi amaçladık. Gereç ve Yöntem: İnsan MM hücre dizisi ARH77 standart kültür kosulları altındadeğisen konsantrasyonlarda (10-7- 10-10 M) ve değisen sürelerde (24, 48, 72 ve 96saat) vinkristine maruz bırakıldı. Survivin gen ifadesi kantitatif RT-PCR ile belirlendi. İstatistiksel olarak gruplar arası farklar iki oran z testi ile değerlendirildi. Bulgular: 24 ve 96 saat uygulama ile survivin gen ifadesinde artıs belirlenmedi. 48ve 72 saatlik uygulama sonrası görülen gen ifade artısı istatiksel açıdan anlamlı idi. (p

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Cite This Article

ATAÇ, F. B., YURTÇU, E., ŞAHİN, F. İ. (2022). Vincristine induced survivin expression in the human multiple myeloma cell line ARH77. Gazi Medical Journal, Cilt: 20 - Sayı: 2, 72–75. https://ajindex.com/articles/520274

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References (14)

  1. Specht K, Haralambieva E, Bink K et al. Different mechanisms of cyclin D1 overexpression in multiple myeloma revealed by fuorescence in situ hybridization and quantitative analysis of mRNA levels. Blood 2004; 104:1120-1126
  2. Magrangeas F, Lodé L, Wuilleme S et al. Genetic heterogeneity in multiple myeloma. Leukemia. 2005; 19: 191-4
  3. Romagnoli M, Trichet V, David C et al. Signifcant impact of survivin on myeloma cell growth. Leukemia 2007; 21: 1070-1078
  4. Sui M, Fan W. Combination of gamma-radiation antagonizes the cytotoxic effects of vincristine and vinblastine on both mitotic arrest and apop- tosis. Int J Radiat Oncol Biol Phys. 2005; 15: 1151-8
  5. Li F. Survivin study: what is the next wave? J Cell Physiol 2003; 197: 8-29
  6. Margulis V, Lotan Y, Shariat SF. Survivin: a promising biomarker for detection and prognosis of bladder cancer. World J Urol. 2008 26: 59-65
  7. Nakagawa Y, Abe S, Kurata M et al. IAP family protein expression correlates with poor outcome of multiple myeloma patients in association with chemotherapy-induced overexpression of multidrug resistance genes. Am J Hematol 2006; 81: 824-831
  8. Ling X, Bernacki RJ, Brattain MG, Li F. Induction of survivin expression by taxol (paclitaxel) is an early event, which is independent of taxol mediated G2/M arrest, J. Biol. Chem, 2004, 279; 15196-15203
  9. Kawamura K, Yu L, Tomizawa M, Shimozato O, Ma G, Li Q, Sato A, Yang Y, Suzuki T, Abdel-Aziz NM, Tagawa M. Transcriptional regulatory regions of the survivin gene activate an exogenous suicide gene in human tumors and enhance the sensitivity to a prodrug. Anticancer Res. 2007 27(1A): 89-93
  10. Carter BZ, Kornblau SM, Tsao TM et al. Caspase-independent cell death in AML: caspase inhibition in vitro with pan-caspase inhibitors or in vivo by XIAP or Survivin does not affect cell survival or prognosis. Blood 2003; 102: 4179-4186
  11. Gooding RP, Bybee A, Cooke F et al. Phenotypic and molecular analysis of six human cell lines derived from patients with plasma cell dyscrasia. Br J Haematol 1999; 106: 669-681
  12. Muto A, Nakagawa A, Shimomura Y et al. Antineoplastic agents for pediatric anaplastic large cell lymphoma: Vinblastine is the most effective in vitro. Leuk Lymphoma. 2005; 46: 1489-96
  13. Meng H, Lu C, Mabuchi H et al. Prognostic signifcance and different properties of survivin splicing variants in gastric cancer. Cancer Lett 2004; 216: 147-155
  14. Jimenez-Zepeda VH, Dominguez-Martinez VJ. Vincristine, doxorubicin and dexamethas